A client who has asthma (a reactive airway disease) asks the nurse about the role of leukotrienes in this process. Leukotrienes have which immune response?
Produce the sensation of Itching.
Tighten airway and produce mucous.
Causes formation of bradykinin.
Serves as receptor for antigen.
The Correct Answer is B
Leukotrienes are inflammatory mediators derived from arachidonic acid metabolism, primarily produced by leukocytes (white blood cells) such as mast cells, eosinophils, and basophils. In the context of asthma, leukotrienes play a significant role in the pathophysiology of the disease by contributing to airway inflammation and bronchoconstriction. Here's a breakdown of their immune response:
A) Produce the sensation of itching:
Leukotrienes are not directly involved in producing the sensation of itching. Itching is often associated with histamine release rather than leukotrienes.
B) Tighten airway and produce mucous:
Correct. Leukotrienes are potent bronchoconstrictors that cause smooth muscle contraction in the airways, leading to narrowing (constriction) of the bronchioles. Additionally, they stimulate the secretion of mucus from goblet cells in the airway epithelium, contributing to airway obstruction and mucus production, which are characteristic features of asthma exacerbations.
C) Causes formation of bradykinin:
Bradykinin is a peptide mediator that is generated from the plasma protein kininogen and is involved in vasodilation, pain sensation, and inflammation. Leukotrienes are not directly responsible for the formation of bradykinin.
D) Serves as a receptor for antigen:
Leukotrienes do not serve as receptors for antigens. Instead, they are lipid mediators released in response to various stimuli, including allergens, infections, and irritants, and they act on specific receptors (e.g., leukotriene receptors) to exert their effects, such as bronchoconstriction and inflammation
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is C
Explanation
A) An increase in afterload results in decreased systolic pressure, which creates a decreased cardiac output:
This statement is incorrect. According to the Frank-Starling law, afterload refers to the resistance against which the heart must pump blood during systole. An increase in afterload typically results in increased systolic pressure, not decreased, as the heart works harder to overcome the increased resistance. However, increased afterload can lead to decreased cardiac output due to the increased work of the heart.
B) A decrease in afterload causes the cardiac muscles to hypertrophy, resulting in increased diastolic volume:
This statement is incorrect. A decrease in afterload typically reduces the workload on the heart, which may lead to reverse remodeling and a reduction in cardiac hypertrophy. Increased diastolic volume may occur due to reduced afterload, but it's not the direct result of hypertrophy.
C) An increase in preload results in greater shortening of myocardial fibers, thereby increasing contractility:
Correct. The Frank-Starling law states that an increase in preload (end-diastolic volume or stretch of myocardial fibers) leads to greater overlap of actin and myosin filaments within myocardial fibers during systole. This increased overlap results in stronger myocardial contraction (increased contractility), leading to an increased stroke volume and cardiac output.
D) A decrease in preload results in increasing diastolic muscle fiber length, which impedes contractility:
This statement is incorrect. Preload refers to the degree of stretch of the myocardial fibers at the end of diastole. A decrease in preload would lead to decreased stretch of the myocardial fibers, not increasing diastolic muscle fiber length. Decreased preload typically results in decreased contractility rather than an impediment to contractility due to reduced myocardial stretch.
Correct Answer is B
Explanation
Parkinson's disease (PD) is a neurodegenerative disorder characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra of the basal ganglia. This degeneration leads to a deficiency of dopamine, a neurotransmitter involved in the regulation of movement and coordination. The inability to express oneself, as seen in the client's mumbling, can be attributed to the motor symptoms of PD, particularly bradykinesia (slowness of movement) and hypomimia (reduced facial expression), which result from dopaminergic neuron degeneration.
A) Damage to Broca's area in the temporal lobe of the brain:
Damage to Broca's area typically results in expressive aphasia, which is characterized by difficulty speaking and forming coherent sentences. While speech difficulties can occur in PD, they are primarily due to motor dysfunction rather than damage to specific language centers in the brain.
B) Degeneration of dopaminergic neurons of the basal ganglia:
Correct. Degeneration of dopaminergic neurons in the basal ganglia, particularly the substantia nigra, is the primary pathological factor in Parkinson's disease. This degeneration leads to motor symptoms such as bradykinesia, tremor, and rigidity, which can affect the client's ability to speak clearly and express himself.
C) Brain atrophy with diffuse amyloid plaques disposition:
This description is more characteristic of Alzheimer's disease, a different neurodegenerative disorder characterized by brain atrophy and the deposition of amyloid plaques. While cognitive impairment can occur in PD, the primary motor symptoms are related to dopaminergic neuron degeneration rather than amyloid plaque deposition.
D) Paralysis of the pharyngeal and epiglottal area:
Paralysis of the pharyngeal and epiglottal area can lead to dysphagia (difficulty swallowing) rather than difficulty expressing oneself verbally. While dysphagia can occur in PD, it is not typically the primary factor contributing to speech difficulties in this condition.
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